TIPE2 suppresses angiogenesis and non-small cell lung cancer (NSCLC) invasiveness via inhibiting Rac1 activation and VEGF expression
作者： Zequn Li , Chun Guo , Xianglan Liu , Chengjun Zhou , Faliang Zhu
DOI: 10.18632/ONCOTARGET.11406
关键词: Cancer research 、 Pathology 、 Carcinogenesis 、 non-small cell lung cancer (NSCLC) 、 Metastasis 、 Vascular endothelial growth factor A 、 Tube formation 、 Tumor necrosis factor alpha 、 A549 cell 、 Medicine 、 Angiogenesis
摘要: Non-small cell lung cancer (NSCLC) is one of the leading causes all cancer-related deaths worldwide. Despite extensive efforts to improve diagnosis and treatment this neoplasm, limited progress has been made. Tumor necrosis factor (TNF)-alpha-induced protein 8-like 2 (TIPE2 or TNFAIP8L2) a newly introduced negative immune regulator, which also controls tumorigenesis. However, role TIPE2 in angiogenesis unknown. In present study, we investigated expression roles NSCLC. upregulation human NSCLC tissues was negatively associated with primary tumor size, lymph node metastasis, advanced clinical stage, can be used predict metastasis. Moreover, overexpression not only inhibited colony formation, migration, invasion cells but indirectly suppressed proliferation, tube formation vascular endothelial cells. Furthermore, invasiveness via inhibiting activation Rac1 subsequently weakening its downstream effects, including F-actin polymerization VEGF expression. Collectively, these results indicate that plays key suggesting forced might novel strategy for
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